Abstract
BackgroundAlterations of glucose homeostasis have been reported to occur even in non-diabetic patients, thus increasing the risk of cardiovascular events and worsening the outcome after an acute myocardial infarction (AMI). Still debated is the role of impaired glucose control in patients undergoing percutaneous coronary intervention (PCI), as hyperglycemia, represents an important pro-thrombotic stimulus, increasing platelet reactivity and potentially procedural complications. Therefore, the aim of our study was to assess the association between glycosylated hemoglobin and periprocedural myocardial infarction (PMI) in non-diabetic patients undergoing PCI. MethodsWe included patients without history of diabetes undergoing elective PCI. PMI was defined as creatine kinase-MB increase by 3 times the upper limit normal or by 50% of an elevated baseline value, whereas periprocedural myonecrosis as Troponin I increase by 3× ULN or 50% of baseline. ResultsOur population is represented by 1199 patients, who were divided according to tertile values of glycosylated hemoglobin (HbA1c). Higher HbA1c was associated with ageing (p<0.001), hypertension (p=0.005), previous myocardial infarction (p=0.009), PCI (p<0.001) or CABG (p=0.001), treatment with diuretics (p<0.001), higher levels of glycemia (p<0.001) and white blood cells (p=0.02), multivessel coronary artery disease (p=0.03), higher rate of instent restenosis (p=0.02).HbA1c did not impact on periprocedural myocardial infarction (p=0.85; adjusted OR [95% CI]=0.91 [0.74–1.12], p=0.38) or myonecrosis (p=0.69; adjusted OR [95% CI]=0.95 [0.80–1.13], p=0.56). Similar results were obtained fasting glycemia for PMI (p=0.82, adjusted OR [95% CI]=0.90 [0.71–1.14], p=0.37) and myonecrosis (p=0.21, adjusted OR [95% CI]=1.02 [0.84–1.24], p=0.84) and confirmed in high-risk subsets of patients. ConclusionsIn non-diabetic patients undergoing elective PCI, neither glycosylated hemoglobin levels nor fasting glycemia are associated with the risk of periprocedural myocardial infarction and necrosis.
Published Version
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